-------------------------------------------------------------------------------- TITLE: BAROTRAUMA SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: 18 March 1992 RESIDENT PHYSICIAN: Daniel P. Slaughter, M.D. FACULTY: Francis B. Quinn, Jr., M.D. DATABASE ADMINISTRATOR: Melinda McCracken, M.S. -------------------------------------------------------------------------------- "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." BAROTRAUMA Introduction The organs of hearing and balance, as well as the sinus cavities, are well adapted to slow alterations of the atmospheric pressures, stable gas mixtures and limited acceleration forces. Large pressure changes and altered breathing gas mixtures are encountered in undersea or hyperbaric enviroments. Lesser pressure changes and oxygen enriched gas mixtures are encountered in the hypobaric enviroments of flight and aerospace but these are associated with significant changes in gravity and acceleration. Biophysical principles: Humans are exposed to an ambient pressure caused by the mass of the earths atmosphere. With ascent the density of the surrounding gas and therefore the atmospheric pressure decreases. With descent from surface level the gas density and ambient pressure increases. Ascent or descent in the denser, incompressible aqueous environment results in greater pressure changes than similar movement in flight. In fact the greatest pressure change possible with altitude exposures is one ATA (absolute atmosphere) while a diver is exposed to a pressure change of 1 ATA for each 10m of descent. Units of measure are referenced to absolute vacuum or to one's own location (gauge pressure). For example, sea level is 1ATA and 0 gauge pressure. Important Law: Boyles law- P1xV1=P2xV2. Simply put, with a constant temperature the volume of a gas is inversely proportional to the pressure. As one undergoes descent in the ocean the increased pressure will cause compression of the confined volume of air in the middle ear and the paranasal sinuses. Here the action of the eustachian tube and the natural ostia are very important in equalizing these otherwise confined volumes to the external source of compressed gas in the tank. Barotrauma is more likely to occur near sea level. Key principles: In accordance with Boyles Law- both shallow dives and low altitude flights have a greater potential for barotrauma. ex. Sea level is 1ATA and a descent to 10 meters (33ft) is 2ATA causing the gas volume to be halved; therefore, 20 meters is 3ATA and the volume would be halved again thereby making it 1/4 the original volume. One can see that the greater change in volume occurred at the initial 10 meter descent. The same principle applies to ascent but one must remember that a maximum change of 1ATA is possible with ascent from sea level. Example: In flying at an altitude of 18,000 feet above sea level the pressure is 1/2 that of sea level, and the pressure halves again at 34,000 feet and again at 48,000ft. The greatest change in pressure occurred at the initial 18000 ft. Although it is true that ascent in aircraft causes much less absolute pressure change, the rapidity and fluctuation can make accommodation quite difficult. Aircraft reduce this hazard by maintaining the aircraft cabin pressure at a more physiological level. Simply put the "gauge" pressure within the cabin is at a lower altitude than the actual plane altitude. Airliners usually fly at 30000 - 40000 ft (226-141mmHg) but keep the simulated cabin altitude at 8000 ft (564mmHg). When the plane descends from 30000 feet to land at sea level (a change of 226mmHg to 760mmHg=534mmHg) the passenger must only adjust from an 8000 ft to sea level (a change of 564 to 760mmHg=196mmHg) Eustachian tube function: The eustachian tube (ET) protects the middle ear cavity from barotrauma when it functions normally. Upon ascent both in diving and in flying the volume in the middle ear expands. As the pressure builds the ET should open allowing equilibration of the air and preventing barotrauma. This passive opening is usually reliable and therefore barotrauma is infrequent in this situation. The reverse is true of descent when the volume of air in the middle ear decreases. Failure or even delay of the ET to open will result in low middle ear pressure and will tend to lock the ET. Further descent after this point will result in barotrauma. The ET is normally collapsed in its resting state and opens with swallowing and yawing. During descent the ET must stay open long enough for the pressure within the middle ear to equilibrate with that of the nasopharynx. Basic variations in tubal lumen size and muscular activity along with inflammatory conditions and masses can result in widely varying " tube opening times". In a rapidly changing barometric environment a "short opening time " can result in barotrauma. Pathological changes of middle ear barotrauma: The pathological changes that occur with middle ear negative pressure vary according to the rate and magnitude of pressure change and include: mucosal hemorrhage and congestion, edema, serous and hemorrhagic effusions ,and infiltration of leucocytes (PMN) within the middle ear mucosa. The inwardly displaced TM also undergoes vascular congestion followed by vessel rupture and interstitial hemorrhage or the formation of bullae. TM rupture most commonly occurs in the anterior portion over the middle ear orifice of the eustachian tube. Significant force may occur as to cause an annulus rupture. Pressure changes as low as 30mmHg have been shown to cause minor barotrauma. Staging systems have been proposed to quantify barotrauma but are difficult to use clinically although they do help describe the sequential damage that usually occurs. Edmonds et al: grade 0 symptoms without signs grade 1 diffuse redness and retraction grade 2 plus slight hemorrhage within the tympanic membrane (TM) grade 3 plus gross hemorrhage within the TM grade 4 dark and slightly bulging TM with free blood in the middle ear and possible air/fluid level grade 5 above plus TM perforation. Prevention: Maneuvers to equilibrate middle ear pressure: Valsalva maneuver (modified)- controlled expiration with the lips closed and the nares pinched. The ET is opened by the elevated nasopharyngeal pressure created by expiration without an outlet. Care must be taken with this method as it has been implicated in round and oval window rupture as is described later in this chapter. Frenzel maneuver - closing the glottis,mouth,nose while simultaneously contracting the floor of the mouth and the superior constrictor muscles. This maneuver actually takes less pressure to open the ET but is more difficult to learn. To attempt one must thrust the lower jaw anteriorly,close your lips,slightly open your jaw, move the mass of the tongue against the soft palate and compress the air in the nasopharyngeal space. There is no reported case of inner ear trauma secondary to this maneuver. Toynbee maneuver - swallowing with a pinched nose. A small initial positive nasopharyngeal pressure rapidly becomes a negative pressure which may help unlock the ET. Historical Factors: Historical factors are probably the best indicators of the risk for barotrauma. History of nasal or middle ear disease, prior otologic surgery, upper respiratory infection (URI), perforation, cholesteatoma. Chronic use of decongestants and nasal sprays. History of previous barotraumatic exposures. Eustachian Tube Tests: Whether there is a simple and accurate test to objectively identify those patients who might develop barotrauma is arguable. Miller described a rather cumbersome technique of evaluating ET function that involved the creation of a positive or negative pressure within the middle ear via the external auditory canal (EAC) and a TM defect. ET function was then assessed by the ability to equalize this pressure with swallowing. The necessity of a TM defect especially in the prediving evaluation is a serious drawback. Williams described a similar test he called the eustachian tube swallow test. This test does not call for a TM defect nor the use of equipment not usually found in an audiology suite. A baseline tympanogram is performed first. The pressure is then increased in the EAC to 400mm water and the patient is asked to swallow several times. A repeat tympanogram is then performed. Subsequently the pressure in the EAC is kept at -400mm water and the patient is again instructed to swallow several times followed by a repeat tympanogram. Interpretation is as follows: with +400mm a mechanical pressure will be generated in the middle ear and with normal ET function air will be forcefully expelled with swallowing. Repeat tympanometry at this time should document that there is a smaller volume of air left in the middle ear and therefore a negative shift should occur. Conversely a -400 results in air being brought into the middle ear with swallowing and therefore a positive shift should occur. Unfortunately the test was only shown to be a predictor of good function but not of poor function. Schuchman showed it to be of no value in a prospective study on scuba students. McBride demonstrated that the 9 step test of the ET (same principle as Williams test) was a good predictor of ET function. Ferneau showed that the 9 step test was an accurate predictor of those people who would develop barotrauma with hyperbaric therapy but no better than historical factors. Shupak also showed that successful autoinflation at sea level does not necessarily reflect middle ear pressure equalization ability during descent in a dive. Preventive measures: Frequent use of equalizing maneuvers, slow descent, predive or preflight use of topical long-acting nasal sprays. Systemic agents are believed to be less useful. Evaluation and management: Initial evaluation must determine if middle and or inner ear damage had occurred. Loud tinnitus, vertigo, nystagmus, bone conduction loss suggest labyrinthine window rupture. Audiogram should be performed in all cases. Symptoms without otoscopic signs: Avoidance until all symptoms are resolved and autoinsufflation can be performed. 5-7 days of a long acting nasal spray is recommended (administered supine with the head in a hyperextended position). Critical evaluation of inciting conditions. Symptoms with signs but no rupture of TM: as above. May require a longer recuperation. Antibiotics probably unnecessary unless purulence noted in the nasopharynx or the patient notices a change for the worse in the pain and/or purulent otitis ensues by exam. Symptoms with TM perforation: Most heal spontaneously. The ear should be cleaned with the microscope to clear debris. Tears can be reapproximated and possibly a paper patch applied to the tear. Lindeman challenged the idea that reapproximation with paper patch was of assistance in a prospective paper and stated that most of the perforations will heal spontaneously and there was no difference in his two groups in healing. Ototoxic GTTS should not be used as there is a possibility of window rupture. Antibiotics should be used for 7-10 days. Delayed middle ear barotrauma: Barotrauma several hours after the completion of a long flight using 100% 02 usually upon awakening . The likely mechanism involves the rapid absorption of the 02 resulting in the development of a negative pressure in the middle ear. The asleep patient does not equilibrate as the negative pressure increases. Phenomenon of end of the day barotrauma- repeated mild barotrauma that asymptomatically results in swelling of the ET eventually results in symptomatic barotrauma as ET function becomes worse. Alternobaric vertigo- this is a well documented syndrome that most frequently occurs during or immediately after ascent from diving. Lundgren first coined the name alternobaric vertigo after a survey of Swedish sport divers. He found that 26% of those surveyed had experienced alternobaric vertigo. Other surveys by Terry and Vorosmarti resulted in 40% and 11.9% incidence. A large survey by the Australian navy revealed an incidence of only 0.4%. The patient feels an initial unequal pressure in the ear followed by dizziness and vertigo. Ingelstedt demonstrate that if a pressure difference of 60cm water pressure develops between the two ears that an increasing labryinthine discharge induces an irritative nystagmus and vertigo. Interestingly many of those divers who reported alternobaric vertigo with diving could reproduce the symptoms by performing a Valsalva maneuver. The episode usually lasts from a few seconds to a 15 minutes. If one begins to develop these symptoms then they need to stop ascent or descent and utilize equalibrating mechanisms until the symptoms resolve. Alternobaric facial paralysis- multiple case reports exist reporting similar episodes of difficultly with middle ear equilibration on ascent and subsequent transient facial paralysis. Theories include: 1) direct barotrauma on a dehiscent tympanic portion of the facial nerve secondary to an overpressurized middle ear space during unequilibrated ascent 2) Over pressurized middle ear during ascent causes bubbles to enter through the chorda fenestrum. Reported cases have all been transient and observation is the treatment advocated. Flying with chronic otitis media with effusion (COME)? Weiss et al performed a prospective study using preflight audios and tympanograms and demonstrated no increase incidence of barotrauma in ears with COME. Interestingly it was the opposite "normal" ears that developed barotrauma in some cases. He postulated that since the ear is filled with fluid instead of a gas that Boyles law and therefore the events outlined above do not apply. It would be in those "normal " ears that still have an air filled space that barotrauma would occur as they probably do have some element of ET dysfunction as documented by contralateral pathology. Inner Ear Barotrauma: Most commonly reported in diving (hyperbaric) conditions although also can be seen during descent in flight. History: In 1962 Simmons postulated the existence of a hearing loss syndrome secondary to mechanical disruption of Reissner's membrane secondary to a rise in intracranial pressure. Stroud and Calcatera (1970) advanced the theory by suggesting that increased perilymphatic pressure might occur throughout the labryinthe with rupture of other membranes other than Reissner's membrane. Goodhill then presented patients with ruptures of the round and oval windows with a history of exertion preceding the loss (1971/1973). Goodhill proposed explosive and implosive mechanisms for inner ear injury. The explosive mechanism states that the middle ear pressure becomes negative relative to intralabrynthine fluid pressure in the presence of inadequate middle ear clearing during descent. A modified Valsalva maneuver may increase the intralabrynthine fluid pressure via the cochlear aqueduct or the IAC but fail to equilibrate the middle ear pressure and therefore increase the differential between the perilymph and the middle ear cavity. Rupture of the round or oval window may then occur causing a perilymph fistula with SNHL and vertigo. Animal studies document that this occurs. The implosive mechanism states that with a sudden, forceful, modified Valsalva a rapid increase in middle ear pressure occurs causing a rupture of the round or oval window and fistula. This mechanism of implosive injury is considered to be much less frequent than the explosive injury. Another theory of implosive injury is that the negative middle ear pressure that can occur in diving may cause inward displacement of the ossicles with subluxation of the stapes footplate and oval window fistula. Stoud and Calcatera, Pullen, Freeman and Edmonds all presented cases documenting the existence of perilymphatic fistulas in diving and related incidents. There have been numerous well documented cases of sudden sensorineural hearing loss (SNHL) after shallow dives where round window fistulas were seen at exploratory tympanotomy. Repair results in improvement in hearing and vertigo in some cases. A high index of suspicion is required to make the diagnosis. Singleton showed certain clinically statistically effective predictors of a perilymph fistula including: sudden onset of postural vertigo and/or hearing loss after a barotrauma incident, multipositional nystagmus, gaze nystagmus, reduced speech discrimination and speech reception threshold (SRT). In general a complete otoneurologic exam, including routine audiometry, tympanometry, SRT, discrimination, ENG, and possibly ABR is indicated in the workup of a patient with post barotrauma SNHL. Management of suspected inner ear barotrauma: All such cases carry in common the barotrauma followed by combinations of SNHL, tinnitus, and vertigo. If you encounter a patient with these symptoms, without a history consistent with decompression sickness, recompression therapy should not be performed as it will aggravate the injury. Recommended therapy includes: bed rest, elevation of the head, avoidance of straining or activities that could increase CSF pressure. The timing of exploratory tympanotomy is controversial. Some would recommend immediate exploration. Most will allow 24-48 hours to observe with exploration if signs of worsening. If no improvement in 4-5 days most would explore. Divers who exhibit persistent inner ear deficits should not return to diving. Differentiating inner ear barotrauma (IEB) from inner ear decompression sickness (IEDS): Both diving related inner ear barotrauma and inner ear decompression sickness can result in permanent severe cochleovestibular deficiency if appropriate diagnosis and treatment is not instituted quickly. The cardinal symptoms of both syndromes are similar and consist of any combination of SNHL, tinnitus, and vertigo. The differential between the two is crucial as their respective treatments would be harmful for the other. The crux of this differential lies in the history and the physical exam. The mechanism of IEB has been detailed above. IEDS is related to the formation and growth of inert gas bubbles within microvessels and the otic fluids, which takes place when ever pressure drops rapidly during the ascent from a dive to a level shallower than that required to keep gas soluble. Consequent blockage of the microcirculation mainly affecting the venous circulation of the stria vascularis, spiral ligament, and the SCC's leading to hemorrhages and protein exudation in the cochlea, as well as to irritation of the endosteum which lines the bony SCC's. The protein exudates and hemorrhage in the cochlea are spontaneously resolved. However, the injury to the bony SCC's endosteum leads to osteoblastic differentiation with infiltration of fibrotic tissue and new bone growth into the SCC spaces. The questions one must asked when confronted with the differentiation of IEB and IEDS are as follows: the dive profile and characteristics including decompression time required, omitted decompression, rapid descent or ascent, and gas mixture used. The onset of symptoms during descent or ascent, or shortly after decompression. Associated symptoms such as other decompression sickness symptoms, difficulty in clearing ears, pre existing otologic complaints , or nasal or sinus complaints. IEB as described in this article usually occurs with shallow dives, on descent, with equalization problems, and forceful valsalvas and is not associated with nonotologic neurologic findings. IEDS usually occurs with deep and prolonged dives that may have omitted appropriate decompression steps, on ascent or shortly after ascent, are not associated with pressure equalization problems during the dive, have associated extraotologic neurologic findings. Unfortunately the world is not full of good historians so the case may not be clear cut. Recompression therapy for IEDS is indicated as soon as the diagnosis is made and is strictly contraindicated in IEB. External auditory canal barotrauma: Obstruction of the external auditory canal by foreign bodies, cerumen, tight fitting caps or ear plugs can result in barotrauma to the EAC and TM. The isolated space in the EAC develops relative negative pressure which can result in edema, hemorrhage etc. Outward displacement of the TM can also result in TM trauma. Treatment is essentially the same as for otitis externa. Functional Endoscopic Sinus Surgery (FESS): The same physical principles that result in barotrauma to the ear also apply to the paranasal sinus cavities. Bolger et al from Wilford Hall discussed repeated sinus barotrauma in aviators and described the usefulness of FESS to return the pilots to active flight status. The trauma most often occurs upon descent much as in ear barotrauma. The natural ostia will more reliably allow the exit of air upon the expansion that occurs during ascent. It is with descent that a negative pressure will develop within the sinus cavities which may help "lock" the natural ostia especially in a diseased state and result in barotrauma. Evaluation and treatment for an acute episode of sinus barotrauma is similar to that with acute sinusitis with decongestants and antibiotics. Repeated barotrauma should be evaluated with computed tomography (CT) scan and FESS performed if indicated. ---------------------------------END--------------------------------------